Key result
Oxygen breathing at 1 and 3 ATA increased baroreflex effectiveness compared to atmospheric air, whereas extreme hyperoxia at 5 ATA suppressed the baroreflex mechanism in awake rats.
Why the study?
Cardiovascular responses to hyperoxia include vasoconstriction, bradycardia, and decreased left ventricular contractility, but whether these responses are components of the baroreflex regulating blood pressure and circulation in hyperoxia was unknown.
In a rat model, hyperoxia triggers adaptive baroreflex responses to restrain excess oxygen delivery, though extreme hyperoxia (5 ATA) suppresses this mechanism unless the GABAergic system is activated.
May warrant caution with extreme hyperoxia; leaves open GABAergic baroreflex modulation for translational research.
The cardiovascular system of vertebrates, including humans, is well known to respond to hyperoxia by vasoconstriction, bradycardia and decreased contractility of the left heart ventricle. We hypothesized that all of these responses are components of the baroreflex that regulates blood pressure and circulation in hyperoxia. To test this hypothesis, we carried out experiments on awake rats in which the dynamics of arterial blood pressure, organ blood flow (brain, kidney, lower limbs) and ECG was tracked in response to oxygen breathing at 1, 3 and 5 ATA. The afferent and efferent baroreflex pathways were studied using denervation of the carotid baroreceptors and transection of the aortic depressor nerves and vagus nerve. The baroreflex effectiveness was assessed using phenylephrine injections or spontaneous changes in blood pressure. To activate the GABAergic system, nipecotic acid was injected into the lateral ventricle of the brain. Our studies demonstrated the presence of all the baroreflex components in hyperoxia which were triggered by a sharp rise in blood pressure due to systemic vasoconstriction. Hyperoxic vasoconstriction, in turn, arose due to endothelium-derived nitric oxide (NO) which binds to superoxide anions followed by a loss of the vasodilator component of vascular tone. Aortic and carotid sinus baroreceptors with ascending nerve fibers were identified as an afferent component of the hyperoxic baroreflex. Bradycardia and a decrease in cardiac output, resulting from baroreflex activation by hyperoxia, are actualized via efferent sympathetic and parasympathetic pathways. At 1 and 3 ATA the baroreflex effectiveness increased compared to atmospheric air breathing, but extreme hyperoxia (5 ATA) suppressed the baroreflex mechanism. Activation of the GABAergic system in the cerebral cortex by nipecotic acid prevented the loss of the hyperoxic baroreflex. In hyperoxia, the baroreflex mechanism realizes adaptive responses of the cardiovascular system aimed at restraining the delivery of excess oxygen to an organism and mitigates activation of the sympathetic nervous system.
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Zhilyaev et al. (2019) studied Extreme Hyperoxia. Oxygen breathing vs. Atmospheric air breathing was evaluated on Baroreflex effectiveness and cardiovascular responses. Oxygen breathing at 1 and 3 ATA increased baroreflex effectiveness compared to atmospheric air, whereas extreme hyperoxia at 5 ATA suppressed the baroreflex mechanism in awake rats.
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